Coagulation

Pregnancy is considered a hypercoagulable state increasing the risk of thromboembolic phenomena due to increased venous stasis, vessel wall injury, and changes in the coagulation cascade. The effects of estrogen cause increased synthesis of clotting factors, particularly factors VII, VIII, X, and XII (28). Intra-abdominal vascular stasis secondary to inferior vena cava compression from the uterus also increases the risk of deep venous thrombosis during pregnancy with an incidence of approximately 0.1% to 0.2% (29).

CO2 pneumoperitoneum causes a further increase in venous stasis, which is already present during pregnancy. Jorgensen et al. (30) demonstrated that abdominal insufflation up to 12 mmHg caused a statistically significant decrease in femoral blood flow velocity and an increase in femoral vein diameter, which could not be completely reversed with either intermittent pneumatic compression devices or intermittent electric calf stimulators.

Although pregnancy increases the synthesis of clotting factors, platelets normally decrease during pregnancy, possibly secondary to increased destruction (31,32). Approximately 8% of gravid patients will develop gestational thrombocytopenia with platelet counts between 70,000 and 150,000/mm3. These patients do not appear to experience increased complications and their platelet counts generally normalize by 1-2 weeks postpartum (33).

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